Angiotensis ii
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Angiotensin II: Multifaceted Roles in Cardiovascular and Renal Physiology and Pathophysiology
Angiotensin II and Cardiac Hypertrophy
Key Role in Myocardial Hypertrophy
Angiotensin II (Ang II) is a critical hormone in the progression of myocardial hypertrophy to heart failure. It exerts its effects through the angiotensin-converting enzyme (ACE) and Ang II receptors, which are differentially expressed in cardiomyocytes from neonatal, adult, and failing hearts. The intracellular effects of Ang II are mediated by nitric oxide (NO)/cGMP-dependent cross-talk and the release of autocrine factors such as transforming growth factor (TGF)-beta1 and interleukin (IL)-6. Additionally, Ang II interacts with systemic networks involving aldosterone, parathyroid hormone, and adrenomedullin, which can modify its primary effects.
Angiotensin II in Sepsis
Vasopressor Effects in Hyperdynamic Sepsis
In the context of hyperdynamic sepsis, Ang II has been investigated as a potential vasopressor treatment. Experimental studies in animal models have shown that Ang II infusion can restore arterial pressure, reduce renal blood flow, and significantly increase urine output and creatinine clearance, despite the reduction in renal blood flow. These findings suggest that Ang II can be effective in managing hypotensive hyperdynamic sepsis by improving renal function and maintaining blood pressure.
Angiotensin II and Angiogenesis
Regulation of Angiogenesis
Ang II plays a dual role in angiogenesis through its interaction with AT1 and AT2 receptors. While inhibition of Ang II through ACE inhibitors or AT1 receptor antagonists stimulates angiogenesis, elevated levels of Ang II can also promote angiogenesis via the AT2 receptor. This indicates that Ang II is a humoral regulator of peripheral angiogenesis, with its effects mediated by two receptor subtypes with opposing actions. Additionally, Ang II has been shown to stimulate angiogenesis in the chorio-allantoic membrane of chick embryos, further supporting its role in vascular growth.
Signal Transduction Mechanisms
Complex Intracellular Signaling
The signaling mechanisms of Ang II in vascular smooth muscle cells are complex and involve multiple intracellular pathways. Ang II activates the phospholipase C-diacylglycerol-Ca(2+) axis, tyrosine kinase, and mitogen-activated protein kinase pathways, which do not function independently but engage in cross-talk. These signaling events lead to various physiological and pathophysiological responses, including vascular remodeling and hypertension .
Angiotensin II and Glomerulosclerosis
Induction of Extracellular Matrix Proteins
Ang II contributes to the development of glomerulosclerosis by inducing the expression of TGF-beta, which in turn stimulates the synthesis of extracellular matrix proteins such as biglycan, fibronectin, and collagen type I. This process is mediated by the conversion of latent TGF-beta to its active form and can be blocked by neutralizing antibodies to TGF-beta, highlighting the role of Ang II in renal pathology.
Cardiovascular and Renal Diseases
Pathophysiological Actions
Ang II is central to the pathophysiology of cardiovascular and renal diseases. It causes cellular phenotypic changes, regulates gene expression of bioactive substances, and activates multiple intracellular signaling cascades in various cell types, including cardiac myocytes, vascular endothelial cells, and renal mesangial cells. These actions contribute to conditions such as cardiac hypertrophy, heart failure, vascular thickening, atherosclerosis, and glomerulosclerosis .
Angiotensin II and Atherosclerosis
Promotion of Atherosclerotic Lesions and Aneurysms
Increased plasma concentrations of Ang II have been shown to promote atherosclerotic lesions and abdominal aortic aneurysms in animal models. These lesions are characterized by lipid-laden macrophages and lymphocytes, and the presence of hyperlipidemia is required for aneurysm formation. This underscores the significant impact of Ang II on vascular pathology in the context of hyperlipidemia.
Conclusion
Angiotensin II is a multifaceted hormone with significant roles in cardiovascular and renal physiology and pathophysiology. Its effects are mediated through complex signaling pathways and interactions with various receptors and systemic networks. Understanding these mechanisms is crucial for developing targeted therapies for conditions such as heart failure, sepsis, glomerulosclerosis, and atherosclerosis.
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